Age-Dependent Decrease of Mitochondrial Complex II Activity in a Familial Mouse Model for Alzheimer's Disease

被引：14

作者：

Emmerzaal, Tim L. ^{[1
]}

Rodenburg, Richard J. ^{[2
]}

Tanila, Heikki ^{[3
]}

Verweij, Vivienne ^{[1
]}

Kiliaan, Amanda J. ^{[1
]}

Kozicz, Tamas ^{[1
,4
]}

机构：

[1] Radboud Univ Nijmegen, Dept Anat, Med Ctr, Donders Inst Brain Cognit & Behav, Nijmegen, Netherlands

[2] Radboud Univ Nijmegen, Med Ctr, Dept Pediat, Radboud Ctr Mitochondrial Med,Translat Metab Lab, Nijmegen, Netherlands

[3] Univ Eastern Finland, AI Virtanen Inst, Kuopio, Finland

[4] Mayo Clin, Dept Clin Genom, 200 First St SW, Rochester, MN 55905 USA

来源：

JOURNAL OF ALZHEIMERS DISEASE | 2018年 / 66卷 / 01期

关键词：

Alzheimer's disease; amyloid beta-peptides; electron transport complex II; electron transport complex IV; mice; mitochondria; AMYLOID PRECURSOR PROTEIN; OXIDATIVE-PHOSPHORYLATION SYSTEM; CYTOCHROME-C-OXIDASE; RESPIRATORY-CHAIN; CHRONIC STRESS; APP/PS1; MICE; COGNITIVE IMPAIRMENT; ENERGY-METABOLISM; BETA; DYSFUNCTION;

D O I：

10.3233/JAD-180337

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Alzheimer's disease (AD) is a severe neurodegenerative disorder for which the exact etiology is largely unknown. An increasingly recognized and investigated notion is the pathogenic role of mitochondrial dysfunction in AD. We assessed mitochondrial oxidative-phosphorylation (OXPHOS) enzyme activities in the APPswe/PS1 Delta E9 mouse model from 4.5 to 14 months of age. We show an age-dependent decrease in mitochondrial complex-II activity starting at 9 months in APP/PS1 mice. Other enzymes of the OXPHOS do not show any alterations. Since amyloid-beta (A beta) plaques are already present from 4 months of age, mitochondrial dysfunction likely occurs downstream of A beta pathology in this mouse model.

引用

页码：75 / 82

页数：8

共 78 条

[1] Mitochondrial targeting and a novel transmembrane arrest of Alzheimer's amyloid precursor protein impairs mitochondrial function in neuronal cells [J].

Anandatheerthavarada, HK ;

Biswas, G ;

Robin, MA ;

Avadhani, NG .

JOURNAL OF CELL BIOLOGY, 2003, 161 (01) :41-54

[2] Alterations in Cerebral Cortical Glucose and Glutamine Metabolism Precedes Amyloid Plaques in the APPswe/PSEN1dE9 Mouse Model of Alzheimer's Disease [J].

Andersen, Jens V. ;

Christensen, Sofie K. ;

Aldana, Blanca I. ;

Nissen, Jakob D. ;

Tanila, Heikki ;

Waagepetersen, Helle S. .

NEUROCHEMICAL RESEARCH, 2017, 42 (06) :1589-1598

[3] Unsuspected task for an old team: Succinate, fumarate and other Krebs cycle acids in metabolic remodeling [J].

Benit, Paule ;

Letouze, Eric ;

Rak, Malgorzata ;

Aubry, Laetitia ;

Burnichon, Nelly ;

Favier, Judith ;

Gimenez-Roqueplo, Anne-Paule ;

Rustin, Pierre .

BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, 2014, 1837 (08) :1330-1337

[4] CONTROLLING THE FALSE DISCOVERY RATE - A PRACTICAL AND POWERFUL APPROACH TO MULTIPLE TESTING [J].

BENJAMINI, Y ;

HOCHBERG, Y .

JOURNAL OF THE ROYAL STATISTICAL SOCIETY SERIES B-STATISTICAL METHODOLOGY, 1995, 57 (01) :289-300

[5] Mitochondrial Complex II: At the Crossroads [J].

Bezawork-Geleta, Ayenachew ;

Rohlena, Jakub ;

Dong, Lanfeng ;

Pacak, Karel ;

Neuzil, Jiri .

TRENDS IN BIOCHEMICAL SCIENCES, 2017, 42 (04) :312-325

[6] Alzheimer's Disease as the Product of a Progressive Energy Deficiency Syndrome in the Central Nervous System: The Neuroenergetic Hypothesis [J].

Blonz, Edward R. .

JOURNAL OF ALZHEIMERS DISEASE, 2017, 60 (04) :1223-1229

[7] Cytochrome c oxidase and mitochondrial F1F0-ATPase (ATP synthase) activities in platelets and brain from patients with Alzheimer's disease [J].

Bosetti, F ;

Brizzi, F ;

Barogi, S ;

Mancuso, M ;

Siciliano, G ;

Tendi, EA ;

Murri, L ;

Rapoport, SI ;

Solaini, G .

NEUROBIOLOGY OF AGING, 2002, 23 (03) :371-376

[8] Functional mitochondria are required for amyloid β-mediated neurotoxicity [J].

Cardoso, SM ;

Santos, S ;

Swerdlow, RH ;

Oliveira, CR .

FASEB JOURNAL, 2001, 15 (06) :1439-+

[9] β-amyloid inhibits integrated mitochondrial respiration and key enzyme activities [J].

Casley, CS ;

Canevari, L ;

Land, JM ;

Clark, JB ;

Sharpe, MA .

JOURNAL OF NEUROCHEMISTRY, 2002, 80 (01) :91-100

[10] Mitochondrial Aβ:: a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease [J].

Caspersen, C ;

Wang, N ;

Yao, J ;

Sosunov, A ;

Chen, X ;

Lustbader, JW ;

Xu, HW ;

Stern, D ;

McKhann, G ;

Yan, SD .

FASEB JOURNAL, 2005, 19 (12) :2040-+

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